title: Enhancement of neutrophil infiltration in the corpus after failure of Helicobacter pylori eradication.
abstract: Neutrophil accumulation plays an important role in Helicobacter pylori-associated gastric mucosal injury. In this study, the mucosal content of myeloperoxidase (MPO), which is a measure of neutrophil accumulation and interleukin-8 (IL-8) was assayed and changes in MPO and IL-8 content were determined before and after H. pylori eradication therapy. Thirty-seven H. pylori-positive patients (11DU/26GU) underwent H. pylori eradication therapy with lansoprazole (30 mg/day, 6 weeks) and amoxicillin (2 g/day, 2 weeks), followed by famotidine (20 mg/day, 8 weeks). H. pylori-infection status was evaluated by routine endoscopic examinations (culture, CLO, histology). Immediately and 8 weeks after cessation of the anti-H. pylori therapy, these tests were repeated. Intragastric urease activity was estimated by delta 13CO2, which was obtained by the [13C]urea breath test (UBT). Mucosal samples were taken and tissue MPO and IL-8 contents were assayed by EIA and ELISA, respectively. Histologic examination was also performed. Among the 37 patients, 21 cases of H. pylori infection were eradicated (56.8%). Intragastric urease activity was dramatically reduced immediately after the anti-H. pylori therapy, whereas, it was re-elevated 8 weeks later in the relapsed cases. Antral MPO content was decreased in the eradicated and relapsed cases. MPO in the corpus was also decreased in the eradicated cases. Nevertheless, it was enhanced (3.5-fold) in the relapsed cases at 8 weeks after therapy. Changes in mucosal IL-8 content were similar to those of MPO. In eradicated cases, neutrophil infiltration is improved in both the antrum and corpus. However failure of eradication therapy results in the enhancement of neutrophil accumulation in the corpus. Further study is necessary to clarify the mechanism of neutrophil accumulation after therapy for H. pylori.
authors.affiliation: Division of Gastroenterology, Second Tokyo National Hospital, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: A
authors.initials: A
authors.lastname: Miyayama
authors.forename: N
authors.initials: N
authors.lastname: Iwai
authors.forename: N
authors.initials: N
authors.lastname: Tsunematsu
authors.forename: M
authors.initials: M
authors.lastname: Oonuki
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Hibi
authors.forename: H
authors.initials: H
authors.lastname: Ishii
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D001706:Biopsy; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy* / Q000382:microbiology* / Q000473:pathology; D015738:Famotidine / Q000627:therapeutic use; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D064747:Lansoprazole; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology*; D009853:Omeprazole / Q000031:analogs & derivatives / Q000627:therapeutic use; D009195:Peroxidase / Q000378:metabolism; D054328:Proton Pump Inhibitors; D013276:Stomach Ulcer / Q000188:drug therapy* / Q000382:microbiology* / Q000473:pathology
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D016209:Interleukin-8; D054328:Proton Pump Inhibitors; D064747:Lansoprazole; D015738:Famotidine; D000658:Amoxicillin; D009195:Peroxidase; D009853:Omeprazole